Findings point the way toward a clinical strategy to mitigate an adverse effect of opioids

Originally published by the Pain Research Forum on February 21, 2017

Opioids are the mainstay of treatment strategies to reduce pain, but withdrawal can be a serious problem when patients stop taking these drugs. However, beyond the recognition that microglia play a role in this phenomenon, little is known about the cellular mechanisms involved. Now, new research shows how microglia contribute to withdrawal in rodents and identifies a potential path toward easing withdrawal in patients.

Using a rodent model of morphine withdrawal, a team led by Tuan Trang, University of Calgary, Alberta, Canada, demonstrates that chronic morphine exposure in rodents increases the expression and activity of pannexin-1 (Panx1), a pore-forming channel on the cell surface of microglia that releases ATP. They find that Panx1 function is increased even further during naloxone-induced withdrawal and that inhibition of the channel with two clinically available drugs reduces withdrawal behaviors, providing the opportunity for immediate therapeutic translation.

“It’s a really nice paper. We’ve known for a while that the immune system contributes to opioid withdrawal, but this paper is the first to investigate the underlying cellular mechanisms,” says Peter Grace, University of Texas MD Anderson Cancer Center, Houston, US, who was not involved in the study.

Read the full article here.